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Am J Physiol Gastrointest Liver Physiol 280: G1197-G1208, 2001;
0193-1857/01 $5.00
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Vol. 280, Issue 6, G1197-G1208, June 2001

Localized pancreatic NF-kappa B activation and inflammatory response in taurocholate-induced pancreatitis

Eva Vaquero, Ilya Gukovsky, Vjekoslav Zaninovic, Anna S. Gukovskaya, and Stephen J. Pandol

Department of Medicine, Veterans Affairs Greater Los Angeles Healthcare System and the University of California, Los Angeles, Los Angeles, California 90073

Transcription factor nuclear factor-kappa B (NF-kappa B) is activated in cerulein pancreatitis and mediates cytokine expression. The role of transcription factor activation in other models of pancreatitis has not been established. Here we report upregulation of NF-kappa B and inflammatory molecules, and their correlation with local pancreatic injury, in a model of severe pancreatitis. Rats received intraductal infusion of taurocholate or saline, and the pancreatic head and tail were analyzed separately. NF-kappa B and activator protein-1 (AP-1) activation were assessed by gel shift assay, and mRNA expression of interleukin-6, tumor necrosis factor-alpha , KC, monocyte chemoattractant protein-1, and inducible nitric oxide synthase was assessed by semiquantitative RT-PCR. Morphological damage and trypsin activation were much greater in the pancreatic head than tail, in parallel with a stronger activation of NF-kappa B and cytokine mRNA. Saline infusion mildly affected these parameters. AP-1 was strongly activated in both pancreatic segments after either taurocholate or saline infusion. NF-kappa B inhibition with N-acetylcysteine ameliorated the local inflammatory response. Correlation between localized NF-kappa B activation, cytokine upregulation, and tissue damage suggests a key role for NF-kappa B in the development of the inflammatory response of acute pancreatitis.

acute pancreatitis; nuclear factor-kappa B; activator protein-1; cytokines; chemokines; inducible nitric oxide synthase


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